Sassetti Christopher M, Rubin Eric J
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Building 1, Room 904, 665 Huntington Avenue, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12989-94. doi: 10.1073/pnas.2134250100. Epub 2003 Oct 20.
Despite the importance of tuberculosis as a public health problem, we know relatively little about the molecular mechanisms used by the causative organism, Mycobacterium tuberculosis, to persist in the host. To define these mechanisms, we have mutated virtually every nonessential gene of M. tuberculosis and determined the effect disrupting each gene on the growth rate of this pathogen during infection. A total of 194 genes that are specifically required for mycobacterial growth in vivo were identified. The behavior of these mutants provides a detailed view of the changing environment that the bacterium encounters as infection proceeds. A surprisingly large fraction of these genes are unique to mycobacteria and closely related species, indicating that many of the strategies used by this unusual group of organisms are fundamentally different from other pathogens
尽管结核病作为一个公共卫生问题很重要，但我们对致病生物结核分枝杆菌在宿主体内持续存在所使用的分子机制了解相对较少。为了确定这些机制，我们几乎对结核分枝杆菌的每个非必需基因进行了突变，并确定了破坏每个基因对该病原体在感染期间生长速率的影响。总共鉴定出194个在体内分枝杆菌生长中特别需要的基因。这些突变体的行为提供了细菌在感染过程中遇到的不断变化的环境的详细情况。这些基因中惊人的一大部分是分枝杆菌和密切相关物种所特有的，这表明这群不寻常的生物体所使用的许多策略与其他病原体有根本的不同。
